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  1. #1
    Join Date
    11-20-10
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    142

    Default Mysterious hypotension

    Dr. Agar, one of our IHD members is having a problem with hypotension that has become quite debilitating for her. She has given me permission to share with you the link to her forum post about this problem:

    http://ihatedialysis.com/forum/index...&topic=26342.0

    I have met Desert Dancer, and she is the picture of health. She is our poster child for good dialysis. She does NHHD. She had a parathyroidectomy at around the new year. She has been on dialysis for only two years. You can read her history in her signature.

    It would not be ethical to ask you to diagnose her from half a world away, and her nephrologist is doing her best, I'm sure, to figure out what's going on. But we are all rather stumped, and I wondered if you've ever had a patient like our Desert Dancer who has had the same difficulty with hypotension. Any ideas you might have would be greatly appreciated. Thank you!

  2. #2
    Join Date
    11-17-09
    Location
    Geelong, Victoria, Australia
    Posts
    413

    Default Re: Mysterious hypotension

    Dear Desert Dancer (via Moose Mum) … sorry, but I do not know what other name to call you by …

    You sound as if you have had a terrible time since your parathyroidectomy ~4months ago and, reading through your clinical sequence at the IHD site, it does seem pertinent that the problems surfaced following, and have persisted since this procedure.

    The gist of the problem seems to be a BP ranging 70s/40s coupled with constant dizziness.

    I am pleased you have had an echocardiogram and that this has been stated as normal … this is a very helpful thing to know … and that all the usual things have been tried. I, too, would have bet on too low a dry weight as the most likely problem … though one might have expected, if anything, a little peri-operative 'weight loss' rather than peri-operative ‘weight gain’ and thus, if anything, a little more volume to remove in the post operative days, not less. But, you have tried raising your dry weight – quite significantly – to no avail.

    Anti-hypertensive drugs (eg: atenolol) were (wisely) ceased – also to no avail. Midrodrine, an anti-hypotensive drug that causes vasoconstriction and that helps to raise blood pressure was tried (also without apparent effect) … though I am glad the echocardiogram had been done to ensure good LV function first, as it (midrodrine) is a drug that demands much respect and needs to be used carefully in well selected hypotensive dialysis patients. It is a drug which I have to say I try not to use at all.

    I am also glad you are having thyroid function tests done – these are important to know and be sure that they remain normal – though it would be unusual to find acute thyroid insufficiency after parathyroid surgery.

    The same can be said for checking adrenal function – though, again, why sudden low adrenal gland function should suddenly occur post-parathyroidectomy is a little obscure.

    I note that sodium modeling has been considered (fairly) but rejected (also fairly), for the reasons you state.

    I can also understand your (sensible) anxiety about this affecting your fistula, vision or other complications from it.

    Indeed, it sounds like Desert Dancer has a caring nephrologist who has done all the things that would be done by us all in these circumstances.

    While the temporal association of the onset of your 'troubles' with your parathyroid surgery is hard to deny, I am sure your nephrologist has considered both the possibilities of (1) a relationship and (2) co-inicentality … though I, too, would still be favouring an inter-relationship with the surgery, given your prior excellent health, BP’s and course.

    Turning back to the parathyroidectomy … as this seems to me where the answer may best lie … there are a few 'observations to make. However, it must please be remembered these following comments are made without any knowledge of the patient and thus must be interpreted only as 'thoughts' - and not as fact or informed opinion.

    That said, there have now been several reports of a 'partner syndrome' to the well known ‘hungry bone syndrome' post-parathyroidectomy.

    I will copy below the text of an abstract which was presented under the internet address of the International Society for Hypertension www.ish.org.il/abstract211211/PTH.pdf ... though tbis site does not give the authors names nor their institution … so I must note that (1) an unauthored/undirected abstract should be interpreted with care, however, (2) I believe the context of it is good (ie: the ISH) and (3) I must apologise to the authors for not quoting and acknowledging their names and/or their institution(s), but I could not locate these.

    THE HUNGRY BONE AND DILATED VESSELS SYNDROME: A CASE SERIES OF SEVERE AND LONGLASTING HYPOTENSION OCCURING IMMEDIATELY AFTER PARATHYROIDECTOMY IN HYPERTENSIVE ESRDPATIENTS

    Objective: Secondary hyperparathyroidism and hypercalcemia have been associated with mild hypertension , while parathyroidectomy usually causes a few mmHg drop in blood pressure (BP). We noticed an unusual (and yet unpublished) occurrence of acute severe hypotension immediately after total or subtotal parathyroidectomy, in severely hyperparathyroid and hypertensive patients on hemodialysis. The hypotension becomes longlasting, sometimes disabling. Our aim was to collect clinical data on these cases in order to understand their pathophysiology.

    Design and Methods: We reviewed dialysis recordings of 5 dialysis centers, looking for symptomatic hypotensive patients who were hypertensive before parathyroidectomy. Three patients were detected: patients were interviewed, their medical charts were analyzed, and sitting and standing blood pressure were measured. For two patients we added measurements of central blood pressure and pulse wave velocity (PWV) using SphygmoCor device.

    Results: Patient characteristics and BP measurement done by us are shown in Table 1. All three patients were on Hemodialysis from young age due to congenital or primary glomerular disorders. All had many years of severe tertiary hyperparathyroidism with resultant Ca++ above 9mg/dl despite treatment. Two patients had BP values around 170-200mmHg systolic despite multiple medications. All three showed abrupt fall in blood pressure, that persisted for months, and in one case for 10 years. Currently,two patients have severe symptomatic hypotension, and one patient has borderline hypotension,and doesn't need his blood pressure medications. On average Ca++ dropped about 3mg/dl after surgery. Patients have evidence of preserved cardiac output, decreased systemic vascular resistance, and, despite being on hemodialysis many years,low PWV, reflecting good arterial elasticity.

    Conclusion: We describe a novel clinical presentation of "hungry bone and dilated vessels" syndrome.We found no evidence of orthostatism or autonomic failure,nor a surgical disruption of the carotid sinus.We documented increased arterial elasticity and decreased resistance. A possible change in intracellular calcium, calcium sensing receptor sensitivity or PTH receptor can explain the hypotension. Thus,calcium supplementation or infusion might be of clinical benefit.


    The abstract is, however, interesting. It cites a review of 5 centres and the identification of a ‘syndrome’ … a syndrome is a word for a grouping of similar, likely related findings … where in 3 patients, severe, long-lasting hypotension post-parathyroidectomy was (1) identified and (2) characterized. These authors (unknown to me) described the findings nicely … and it may be worth your showing this particular abstract to your nephrologist.

    The authors of this report conclude that the profound vascular relaxation and blood vessel dilatation may be in response to changes in intracellular calcium or to changes (a resetting) of calcium sensor sensitivity and that calcium supplementation or calcium infusion might be of benefit … though the abstract does not describe this action as having been either taken nor whether, if it was, if it was a successful measure.

    I have not come across this response myself. However, your description is consistent with the syndrome described by the authors, and the theoretical cause and the solution provided by the authors of the abstract seem plausible.

    ‘Hungry bone syndrome’ is well known. Perhaps these authors are describing a parallel ‘hungry vessel syndrome’ with a profound intra-cellular calcium deficit in the endothelium as the cause.

    Interesting ... and I am grateful to Desert Dancer and MooseMum for raising the topic ... for, even if no certain answer can be given, it is great to have to think about it - and to then try to give a sensible response.

    Up-To-Date gives a reference (from a Japanese group: Shinoda et al: Nephron 1992. 60 (4): 482) … a similar report … and again a calcium-based cause was postulated.

    Other references dot the literature – mainly as case reports or in experimental animal work – that attest to the rare but seemingly substantiated occurrence of a profound and lasting ‘hungry vessel syndrome' (my words) … just like as we see with the much more common and well known ‘hungry bone syndrome’.

    Several questions aren’t answered in any of Desert Dancers ‘posts’ … and these all pertain to her calcium status. Did she indeed have hungry bones? What was the level of calcitriol and calcium replacement post operatively? … a process that we routinely protocol-ise and ensure is renal-physician/endocrinologist supervised and not left to the surgical service alone, aggressively ensuring that all post-parathyroidectomy patients receive Ca ++ and Vit D … noting that, sometimes, extraordinary demands and made for (and supplementation needed) to ensure calcium and active vitamin D replacement is adequate – sometimes for months.

    Finally, we (but, more importantly, Chris Chan and his Canadian team who first described it … see Nephrol Dial Transplant (2004) 19: 714–719) have noted a significant increase in the occurrence of delayed graft function and intra- and post-operative hypotension in the days immediately post transplantation in patients who have been on frequent nocturnal HD (extended hour and frequency) dialysis.

    This is a most interesting finding – and is one that seems quite consistent across the experience of the (now) many units who encourage this dialytic modality.

    The question is … why? The postulates (unproven) as to the cause take two main directions: (1) that only these patients among all dialysis patients are in true sodium balance … all others being in a state of chronic sodium overload … and (2) that ‘something’ that affects vascular tone is ‘different’ – with the postulates centering around 3 potential substances: endothelin, nitric oxide … and calcium!

    Not enough is known to take this further, but it is one little added ‘snippet’ that attests to the vital role that endothelial intra-cellular calcium plays in vascular tone and where disturbances of calcium balance can have profound effects on blood pressure regulation – and , especially in these instances, hypotension.

    One aspect I have not dealt with is a 'solution'!

    I note with interest that she is on NHHD.

    We do not know her dialysis fluid (aka - incorrectly - the dialysate) calcium. This is important.

    We commonly use high calcium 'dialysate' ... with a 'bath' Ca++ concentration of 1.5 or 1.6 mmol.L = I think equivalent to a 3.0 - 3.2 mg/dl. Indeed I would go so far to say that it is mandatory to do so and that 'normal' dialysis fluid calciums of 1.3 mmol/l (? 2.6 mg/dl) are way too low for NHHD and will produce a significantly negative Ca++ balance and a toal calcium deficit. This may not always be seen at the macro-level of the serum but may be only at a cellular calcium level.

    I apologise for my mmol/l v mg/dl problems but the US is the only country in the world that does not use international unit system based on mmol/l and I have trouble with conversions to your older system..

    I presume she is on at least a 1.5 mmol/l (3.0 mg/dl) Ca++ fluid.

    Even more, I would expect her to need even more - probably a 1.75 mmol/l (equivalent, I think, to 3.5 mg/dl) dialysis fluid Ca++ concentration. We have not uncommonly used a 1.75 mmol/l = 3.5 mg/dl concentration as our standard 'bath' for NHHD ... aiming for a pre-dialysis Ca++ level of around 2.45 mmol/l (? is that 4.9 mg/dl) and a post-dialysis Ca++ level of ~2.65 mmol/l (? 5.3 mg/dl) ... ie: mild hypercalcaemia.

    The calcium bath of NHHD must be higher than it is for standard 'conventional' dialysis! No if's, no but's ... must be.

    If she is on a normal 1.3 mmol/l (2.6 gm/dl) ... may I hope not ... or even a 1.5 mmol/l bath Ca++, then her 'hungry bones/hungry vessels' will never have had a ghosts chance of recovery and she will be in continuous negative Ca++ balance. I

    f this is what is happening ... though I suspect she already will be on a high Ca++ dialysate ... then she is likely profoundly hypocalcaemic - if not clinically, at a cellular level - and I would not then be surprised at all by her persisting hypotension!

    We need to know this information to know whether all that 'matters' in this particular case ... or whether it is just comment.

    One final feature of Desert Dancer's symptoms that suggests calcium may be the basic issue here is her observation that

    "... things that used to take me an hour or two now take all day long because I have to rest every 15-20 minutes. I can't talk or chew for more than a minute or so before my throat seizes up ..."

    Calcium plays an important role in muscle function ... and low intracellular calcium is associated with muscle fatigue and with laryngeal spasm or weakness. It also can cause cramp-like spasms in the fingers and toes with exertion - carpo-pedal spasm - and sometimes numbness and tingling sensations in the peripheries and around the lips - though none of these are essential for the diagnosis. It might be interesting to know if she has been checked for a positive Trousseau's sign ... a curling-like spasm in the fingers and at the wrist +/- numbness and tingling in the fingers if a BP cuff is inflated to greater than systolic pressure for a few minutes.

    Do I know the answer for Desert Dancer? … no, I do not.

    Can I make an educated guess that it may lie within this issue … well (a qualified) yes, I think I can ... or have.

    This should be discussed with your managing team. As observed in the referral of this question, no internet answer – patient unseen – should be taken as ‘gospel’ . Only broad concepts (even if then) can be discussed. But, I hope this answer may be of some value to Desert Dancer.
    Last edited by John Agar; April 23, 2012 at 03:43 AM.

  3. #3
    Join Date
    11-20-10
    Posts
    142

    Default Re: Mysterious hypotension

    Calcium. Never occurred to me that calcium (LOW calcium) might be the culprit. How fascinating! Thank you. Once again, you have taken a complex concept and managed to explain it so that even a renally impaired brain like mine can grasp it. I understand that this is not a diagnosis, that the patient was unseen and that your post merely presents a well-supported hypothesis. Again, my thanks.

  4. #4
    Join Date
    11-17-09
    Location
    Geelong, Victoria, Australia
    Posts
    413

    Default Re: Mysterious hypotension

    Yes ... Please remember that I do not know the patients who post at this site - I am half the world away - and, thus, any response I might make must always be read with the understanding that any advice given by anyone over the net is never as good as that which is received from a physician who knows the patient, and who knows that particular patients' detailed medical history and record.

    Anything I might say 'here' must be interpreted in this light and must always discussed with the treating team - who may have information that negates some or all of my comments and/or yields them incorrect.

  5. #5
    Join Date
    07-28-11
    Posts
    6

    Default Re: Mysterious hypotension

    Dr. Agar, I must thank you from the bottom of my heart for taking so much time out of your day to provide such a long and detailed response. I cannot tell you how much I appreciate it and I think you have some very lucky patients.

    I just wanted to let you know that I copied the bulk of your response to my nephrologist via email this morning, less than three hours ago. Apparently you made quite the convincing argument because she is increasing the calcium in my bath from 2.5 to 3.0 as of today! It has always been 2.5 and I was only on calcium supplements for one week following my parathyroidectomy. So we will get to test the calcium-based theory.

    A fervent thanks also to MooseMom for posting my dilemma here and getting the ball rolling. If this increase in calcium takes care of my hypotension both you and she will deserve all the credit for it.

  6. #6
    Join Date
    11-17-09
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    Geelong, Victoria, Australia
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    Default Re: Mysterious hypotension

    Thanks - but let's see if calcium is the problem first.

    But, my postulating that the problem lies in your calcium balance is, I must say, my best shot ... and, if I am right, your total calcium deficit may be far, far greater than you think.

    First ... as regards the calcium requirements of the dialysate, Andreas Pierratos from Toronto – the ‘father’ of modern extended hour and frequency dialysis – was the first to draw attention to the need … no, the absolute necessity … of a higher than normal dialysate calcium in patients undergoing long hour, frequent dialysis programs.

    Bob Lindsay and his team from London, Ontario, wrote on this topic in J Am Soc Nephrol 14: 2322–2328, 2003

    … found at jasn.asnjournals.org/content/14/9/2322.full.pdf

    Nigel Toussaint from our own service has published widely on the topic of dialysate calcium: one pare can be found in …

    Hemodialysis International 2006; 10:326–337

    … while the abstract of another paper of ours, also published in HDI and written by Nigel Toussaint when he was our Fellow, is printed below:

    Toussaint ND, Polkinghorne KR, Kerr PG, Somerville CA, Agar JWM. Hemodial Int 2007. 11 (2): 217-224

    Comparison between different dialysate calcium concentrations in nocturnal hemodialysis.

    Abstract
    Benefits of dialysate with greater calcium (Ca) concentration are reported in nocturnal hemodialysis (NHD) to prevent Ca depletion and subsequent hyperparathyroidism. Studies with patients dialyzing against 1.25 mmol/L Ca baths demonstrate increases in alkaline phosphatase (ALP) and parathyroid hormone (PTH) and increasing dialysate Ca subsequently corrects this problem. However, whether 1.5 or 1.75 mmol/L dialysate Ca is most appropriate for NHD is yet to be determined, and differences in the effect on mineral metabolism of daily vs. alternate daily NHD have also not been well defined. We retrospectively analyzed mineral metabolism in 48 patients, from 2 institutions (30 at Monash and 18 at Geelong), undergoing home NHD (8 hr/night, 3.5-6 nights/week) for a minimum of 6 months. Thirty-seven patients were dialyzed against 1.5 mmol/L Ca bath and 11 patients against 1.75 mmol/L. We divided patients into 4 groups, based on dialysate Ca and also on the hours per week of dialysis, <40 (1.5 mmol/L, n=29 and 1.75 mmol/L, n=8) or > or =40 (n=4 and 7). We compared pre-dialysis and post-dialysis serum markers, time-averaged over a 6-month period, and the administration of calcitriol and Ca-based phosphate binders between 1.5 and 1.75 mmol/L Ca dialysate groups. Baseline characteristics between all groups were similar, with a slightly longer, but non-significant, duration of NHD in both 1.75 mmol/L dialysate groups compared with 1.5 mmol/L. The mean pre-dialysis Ca, phosphate, and Ca x P were similar between the 1.5 and 1.75 mmol/L groups, regardless of NHD hr/week. Post-dialysis Ca was significantly greater, with 1.75 vs. 1.5 mmol/L in those dialyzing <40 hr/week (2.64+/-0.19 vs. 2.50+/-0.12 mmol/L, p=0.046), but post-dialysis Ca x P were similar (2.25+/-0.44 vs. 2.16+/-0.29 mmol(2)/L(2), p=0.60). Parathyroid hormone was also lower with 1.75 vs. 1.5 mmol/L baths in the <40 hr/week groups (31.99+/-26.99 vs. 14.47+/-16.36 pmol/L, p=0.03), although this difference was not seen in those undertaking NHD > or =40 hr/week. Hemoglobin, ALP, and albumin were all similar between groups. There was also no difference in vitamin D requirement when using 1.75 mmol/L compared with the 1.5 mmol/L dialysate. Multivariate analysis to determine independent predictors of post-dialysis serum Ca showed a statistically significant positive association with pre-dialysis Ca, dialysate Ca, and total NHD hr/week. An elevated dialysate Ca concentration is required in NHD to prevent osteopenia but differences in serum markers of mineral metabolism between 1.5 and 1.75 mmol/L Ca dialysate in NHD in our study were few. This was similar for patients undertaking NHD <40 or > or =40 hr/week, although differences in the frequency of NHD may also be as important as dialysate Ca with regard to serum Ca levels. With concerns that prolonged higher Ca levels contribute to increased cardiovascular mortality, the optimal Ca dialysate bath is still unknown and further studies addressing bone metabolism with larger NHD numbers are required.


    Your nephrologist will have to do the multiple conversions of dialysate Ca++ in this abstract but, essentially, calcium in mmol/l is multiplied by 2 to get the equivalent value in mg/dl.

    My guess is that you may need more calcium than even a 3 bath will provide. Here in Australia, most extended hour and fequency dailysis is done against a 3.2 (1.6 mmol/l) dialysate.

    Second ... I think you are likely quite cellularly deplete and will soak up a lot of Ca++ before full correction occurs or until your symptoms abate. so ... don't look for an overnight 'cure' ... if calcium is the problem - I think it likely is - then improvement will be gradual and your strength and vascular tone may take some weeks to recover. As it does, however, I would hope you might improve progressively back to your previous state of health.

    You may likely also need supplemental Vit D in the form of calcitriol ... and more than just daily ... along with oral Ca++ for a time, until you calcium balance turns from negative to positive. We use a protocol post-parathyroidectomy that pours in calcium ... with often as many as 0.5 ugm calcitriol qid and calcium IV then oral out, often, for several weeks - though different people have different calcium and calcitriol needs and this is clearly influenced by frequent measurements of the serum calcium to gauge (1) how much and (2) how long.

    I am glad you have run this past your nephrologist - as you must - as there are many pitfalls in Internet diagnosis and this is not and cannot be a replacement for your physicians care and advice.

    In time, please let me (and others) know how you went and ...

    (1) if a calcium deficit proved to be the underlying problem

    (2) if you recovered after calcium repletion.
    Last edited by John Agar; April 25, 2012 at 12:41 AM.

  7. #7
    Join Date
    05-02-12
    Posts
    2

    Default Re: Mysterious hypotension

    Good day, Dr. Agar - like DesertDancer, I too have been experiencing hypotension, but with a bit different background. Below are my posts from the IHD thread. I would appreciate suggestions as well. Thank you in advance - NoahVale

    "I was born with a urinary problem that wasn't corrected until 12 y.o. By that time, most of my kidney function had been destroyed. I started on dialysis at 22, received a transplant at 34, and back on dialysis in 2004 at 48 - 20 1/2 years of dialysis total.

    I've had no other medical complications except those related to renal failure. Been slim and smallish my whole life. While on dialysis the first go round I stayed as active as any "normal" person. In fact, if not for access problems, probably would not have had a transplant for another 10 years. Though, don't get me wrong, the first 13 years of my transplant I experienced absolutely no problems. Life was good without dialysis and I never looked back.

    Around mid-2009 my BP started to drop from an average of 110/70 (non dialysis days) to 80-85/65-60. Nothing had changed in my day to day regimen. My neph suggested keeping an extra kilo of fluid on and dialing down the dialysate temp. to 35.5 which could help keep BP from bottoming out even more. This worked for a while, but my pressure pre - during - post dialysis was still in the 85-95/60-70 range. Pre-dialysis, my heart rate was around 80-88 and 110-120 post treatment.

    No one was giving me any answers except "you're too dry," so I just learned to live with it. I would not get up or out of bed too quickly. While still getting along with daily routines, it would be at a slower pace.

    Then in the spring of 2010, my BP REALLY took a dip. I told a customer of mine who is a cardiologist what was happening and he had me come in for an eval and tests. I had an ECG, echo cardiogram, and treadmill stress test. All came back negative. My cardiologist diagnosed my problem as venous pooling and put me on 5 mg. of Midodrine x2 daily and told me to wear support socks. The Midodrine didn't help very much because 6 weeks later my pressure REALLY, REALLY bottomed out after a treatment and the next day, the vision in my left eye was impaired.

    I went to a optho-neurologist who said the blood vessels to the eye had been compromised because of the low BP. He wanted me to see a neurologist for an MRI/MRA just to make sure I hadn't also experience a stroke. The scans came back negative as well. Unfortunately, the 50% vision I lost in my eye will not come back. Very hard getting used to - especially peripherally. The upside, I'm a more cautious driver!

    OK, after all this testing, with all showing negative for disease, what next? My neph raised my Midodrine to 10 mg. x2 a day and wanted me to keep an additional kilo of fluid on as long as it was not affecting my lungs, etc. He also stated that this was not an uncommon condition for long-term dialysis patients and should reverse once re-transplanted.

    Well, like yourself, I had started eating Midodrine like M&Ms because I was becoming sensitized to the med. Yet, taking 50 mgs. a day, my pressure wasn't going higher than 90/60. Then last summer, my liver enzymes started going out of whack. I stopped all meds except for Fosrenol and baby aspirin, and made an appt. with a gastroenterologist considered the "doctor's doctor" here in Atlanta. Another round of blood tests and scans. He could find no explanation except for the Midodrine. And, since I stopped taking it, my liver enzymes have dropped back (except Alk. Phos. which also has to do with renal bone disease).

    So, here I was - take tons of midodrine with minimal help and experience liver damage or stop and live with the effects of low BP. I chose the latter. I also decided to slowly challenge lowering my dry weight. Fluid tends to gather in my abdominal area and is the hardest to remove. Over the last 9 months I have taken maybe 3 - 10 mg. pills of midodrine, dropped by dry weight by 2 k, while maintaining an average pre-dialysis BP of 90-95/60-65. Even with the lower dialysate temp. and sodium modeling, my BP still drops about 15 points systolic on initiation of dialysis. But, it does go up during tx (I run incenter, extended hours). I also believe my compromised vascular system from the numerous access surgeries over the years plays into the BP problem as well....

    I had a parathyroidectomy around Christmas, 1989. Don't remember having low BP afterwards, but did have to greatly increase my calcium intake. Also remember after my transplant in June, 1990, I experienced hypocalcemia and was on tons of IV calcium. High steroid doses immediately post transplant and low PTH from the parathyroidectomy were the causes. Took about 4 weeks before the IV infusions were discontinued, but I had to stay on oral calcium supplementation for a few more months.

    ...I have been running on a 3.0 Ca / 2.0 K bath for quite some time. I'm going to ask my neph if the Ca can be raised to 3.5. Being in center, that might not be an option. Also, since going back on dialysis in 2004 my PTH has remained in the 60-90 range with no vitamin d therapy (must still be getting some residual function from my transplant). For the past 4 years my serum Ca level as been running in the 8.2-8.9 range. I'm going to try and get it within the 9.0-9.3 range to see if that helps with BP.

    While I never had the feeling my MDs were not taking my condition seriously enough, like yourself, I did research on the causes of low BP. I too thought adrenal gland problems, but my neph ordered a blood serum Aldosterone test and it came back normal. I'm also not diabetic.

    I'm scared too about losing my graft since my access options are about out. However, with my BP stabilized in the 90/60 range and running extended hours w/a 300 blood speed and dialysate temp. of 35.5, I feel less worried."
    Last edited by Noahvale; May 3, 2012 at 09:27 AM.

  8. #8
    Join Date
    11-17-09
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    Geelong, Victoria, Australia
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    Default Re: Mysterious hypotension

    Noah ...

    Here's a 'sort of' response to some of the salient points in you post. Please dont take these comments as 'real' medical advice ... they are not meant that way, but just thoughts, as you went along, about your problem.

    Only your doctor, who has done all the right things for you in my view, can properly advise you as he knows all your circumstances - and knows you ... I do not.


    Now to your post ...

    "I was born with a urinary problem that wasn't corrected until 12 y.o. By that time, most of my kidney function had been destroyed. I started on dialysis at 22, received a transplant at 34, and back on dialysis in 2004 at 48 - 20 1/2 years of dialysis total.

    I've had no other medical complications except those related to renal failure. Been slim and smallish ...

    If I may venture to say, probably because your growth slowed as a result of your childhood kidney troubles ...

    ... my whole life. While on dialysis the first go round I stayed as active as any "normal" person. In fact, if not for access problems, probably would not have had a transplant for another 10 years. Though, don't get me wrong, the first 13 years of my transplant I experienced absolutely no problems. Life was good without dialysis and I never looked back.

    You have certainly had your share of trials, Noah ...

    Around mid-2009 my BP started to drop from an average of 110/70 (non dialysis days) to 80-85/65-60. Nothing had changed in my day to day regimen. My neph suggested keeping an extra kilo of fluid on and dialing down the dialysate temp. to 35.5 which could help keep BP from bottoming out even more.

    A good initial suggestion, I suspect, at the time ..

    This worked for a while, but my pressure pre - during - post dialysis was still in the 85-95/60-70 range. Pre-dialysis, my heart rate was around 80-88 and 110-120 post treatment.

    This still suggests that you were volume contracted.

    I would probably have done an echocardiogram at this point – given your long history of CKD, dialysis and transplantation – but I note that this was done a year or so later by your cardiologist, along, appropriately, with a stress test (though, maybe, I would have combined the two at the time into a stress echo) ... and these are not particularly critical differences in approach...


    No one was giving me any answers except "you're too dry," so I just learned to live with it. I would not get up or out of bed too quickly. While still getting along with daily routines, it would be at a slower pace.

    Then in the spring of 2010, my BP REALLY took a dip. I told a customer of mine who is a cardiologist what was happening and he had me come in for an eval and tests. I had an ECG, echo cardiogram, and treadmill stress test. All came back negative.

    At this point, I would have wanted to know more about your adrenal axis ... maybe even earlier. You presumably will have had a significant steroid exposure during your transplant years and endogenous production (ie: you own adrenal gland production of steroid hormones as opposed to exogenous – medication delivered steroid) would have been long-time suppressed.
    It is possible that you are (or have been) exhibiting evidence for endogenous steroid depletion ... an insidious syndrome known as hypoadrenalism (or Addison’s disease) ... so I would have wanted to know more about your cortisol production and might have at this stage – after measuring all your adrenal function (and not just the Aldosterone levels you later have had measured) – then, popssibly, I’d have trialed you on fludrocortisone.


    My cardiologist diagnosed my problem as venous pooling and put me on 5 mg. of Midodrine x2 daily and told me to wear support socks. The Midodrine didn't help very much because 6 weeks later my pressure REALLY, REALLY bottomed out after a treatment and the next day, the vision in my left eye was impaired.

    As I have already commented, I am not a particular fan of midrodrine – but that was said in a previous post in this thread

    I went to a optho-neurologist who said the blood vessels to the eye had been compromised because of the low BP. He wanted me to see a neurologist for an MRI/MRA just to make sure I hadn't also experience a stroke. The scans came back negative as well. Unfortunately, the 50% vision I lost in my eye will not come back. Very hard getting used to - especially peripherally. The upside, I'm a more cautious driver!

    OK, after all this testing, with all showing negative for disease, what next? My neph raised my Midodrine to 10 mg. x2 a day and wanted me to keep an additional kilo of fluid on as long as it was not affecting my lungs, etc. He also stated that this was not an uncommon condition for long-term dialysis patients and should reverse once re-transplanted.

    Well, like yourself, ... here I suspect you are referring to Desert Dancer, who initiated this thread, and not to me ... I had started eating Midodrine like M&Ms because I was becoming sensitized to the med. Yet, taking 50 mgs. a day, my pressure wasn't going higher than 90/60. Then last summer, my liver enzymes started going out of whack. I stopped all meds except for Fosrenol and baby aspirin, and made an appt. with a gastroenterologist considered the "doctor's doctor" here in Atlanta. Another round of blood tests and scans. He could find no explanation except for the Midodrine. And, since I stopped taking it, my liver enzymes have dropped back (except Alk. Phos. which also has to do with renal bone disease).

    I am glad the midrodrine was ceased ... it can be nasty stuff ... and I dont think it works too well, either.

    So, here I was - take tons of midodrine with minimal help and experience liver damage or stop and live with the effects of low BP. I chose the latter. I also decided to slowly challenge lowering my dry weight. Fluid tends to gather in my abdominal area and is the hardest to remove. Over the last 9 months I have taken maybe 3 - 10 mg. pills of midodrine, dropped by dry weight by 2 k, while maintaining an average pre-dialysis BP of 90-95/60-65. Even with the lower dialysate temp. and sodium modeling, my BP still drops about 15 points systolic on initiation of dialysis. But, it does go up during tx (I run incenter, extended hours). I also believe my compromised vascular system from the numerous access surgeries over the years plays into the BP problem as well....

    I take it that the sodium modelling didnt help ... in my view, despite its theoretical promise and value, it rarely does.

    I had a parathyroidectomy around Christmas, 1989. Don't remember having low BP afterwards, but did have to greatly increase my calcium intake. Also remember after my transplant in June, 1990, I experienced hypocalcemia and was on tons of IV calcium. High steroid doses immediately post transplant and low PTH from the parathyroidectomy were the causes. Took about 4 weeks before the IV infusions were discontinued, but I had to stay on oral calcium supplementation for a few more months.

    I think that many people – professionals and patients alike – underestimate the calcium deficit and the sometimes massive amount of calcium and ‘D’ replacement that is needed after parathyroidectomy.

    Desert Dancer – whose plight triggered this thread – may need way, way more than she has had – or even now is receiving. Her Ca++ replacement, via the (only) modest increase in dialysate Ca that has been prescribed for her, may need to be much more than she is getting – even now – to achieve a positive calcium balance ... a status I think she may still remain far away from achieving.

    Your post-parathyroidectomy calcium deficit seems to have been well replaced and your treatment with ‘tons’of IV calcium is our common experience too.
    ...

    I have been running on a 3.0 Ca / 2.0 K bath for quite some time. I'm going to ask my neph if the Ca can be raised to 3.5.

    Provided that your post Ca++ levels do not creep too high (not more than about 2.7 mmol/l), and your Ca/PO4 product stays nicely low, that would be fine. We always aim for - and achieve - a product of less than 3 in our extended hour 5 x 8-9 hr/week patients ... remembering that we work here in mmo/l and that our normal range for calcium in SI units = 2.15 – 2.55 and for phosphate = 0.75 – 1.4 mmol/l.

    Your nephrologist would need to help you to make the equivalent conversion.


    Being in center, that might not be an option.

    I hope that is not the case. One windmill I tilt at is the ‘one-size-fits-all’ dialysis model ... all patients are NOT the same. Individual dialysis prescritions are needed to overcome individual needs and it should be possible to accommodate a range of dialysate variations in any unit. In my view, it is indefensible not to do so, if dialysate or other prescription individualizations are indicated – as they very often are.

    Also, since going back on dialysis in 2004 my PTH has remained in the 60-90 range with no vitamin d therapy (must still be getting some residual function from my transplant). For the past 4 years my serum Ca level as been running in the 8.2-8.9 range. I'm going to try and get it within the 9.0-9.3 range to see if that helps with BP.

    It may ... but I would be interested to know if an endocrinologist might delve a little more into your adrenal axis first. While I suspect Ca++ may be Desert Dancers’ issue, it is, to be honest, less likely yours, given the good post-parathyroidectomy Ca++ replacement you seem to have received.

    While I never had the feeling my MDs were not taking my condition seriously enough, like yourself, I did research on the causes of low BP. I too thought adrenal gland problems, but my neph ordered a blood serum Aldosterone test and it came back normal. I'm also not diabetic.

    I am not sure an Aldo level, alone, is enough. Maybe a little deeper adrenal delving ...?

    I'm scared too about losing my graft since my access options are about out. However, with my BP stabilized in the 90/60 range and running extended hours w/a 300 blood speed and dialysate temp. of 35.5, I feel less worried."

    If you are feeling OK, thats not such a bad combination ... though I still might be thinking about your volume and your adrenals a bit more. Does your team have access to a BCM = body composition monitor? ... I am sure you will have had a BVM assessment but the BCM can also provide useful additional information.

    One final comment – I have assumed (though one should never assume) that your albumin has been normal throughout and remains normal.
    Last edited by John Agar; May 4, 2012 at 02:41 AM.

  9. #9
    Join Date
    05-02-12
    Posts
    2

    Default Re: Mysterious hypotension

    Dr. Agar, I appreciate your quick and thoughtful response. I look upon your comments as a resource tool in helping to determine how to treat my medical problem.

    Yes, the onset of kidney problems, pre-puberty, did stunt my growth development to some extent. I'm 5'8' and 140 lb., but small-boned.

    At this point, I would have wanted to know more about your adrenal axis ... maybe even earlier. You presumably will have had a significant steroid exposure during your transplant years and endogenous production (ie: you own adrenal gland production of steroid hormones as opposed to exogenous – medication delivered steroid) would have been long-time suppressed.
    It is possible that you are (or have been) exhibiting evidence for endogenous steroid depletion ... an insidious syndrome known as hypoadrenalism (or Addison’s disease) ... so I would have wanted to know more about your cortisol production and might have at this stage – after measuring all your adrenal function (and not just the Aldosterone levels you later have had measured) – then, popssibly, I’d have trialed you on fludrocortisone.
    - I will follow up further on this suggestion. However, my 1 year post-transplant daily medication regimen was fairly low: 5mg. Prednisone/250mg. Cya/75mg. Imuran. Although there are 2 transplant programs where I live (Atlanta), I chose the UAB program under Gil Diethelm's direction at that time. I liked his attitude of having patients take the least amount of meds to keep their grafts working as opposed to the Atlanta programs' philosophy of taking as much as can be tolerated. I knew with pre-adolescent onset of kidney failure high doses of steroids would lead to hip/knee replacements. I remember Dr. Diethelm telling me that I could stop the prednisone altogether after about a year post transplant. I "compromised" by staying on 5mg. - thinking a low dose wouldn't hurt and could help keep the graft going. He, too, mentioned the amount of endogenous production.

    I take it that the sodium modelling didnt help ... in my view, despite its theoretical promise and value, it rarely does. - I still use it with a starting Na of 147 and ending 137, stopping with 30 minutes left in treatment. I believe that, and long with the lower dialysate temp., helps from midway through treatment on. At least it doesn't hurt.

    Does your team have access to a BCM = body composition monitor? ... I am sure you will have had a BVM assessment but the BCM can also provide useful additional information. - I don't know. Another point I will bring up.

    One final comment – I have assumed (though one should never assume) that your albumin has been normal throughout and remains normal. - Yes, my serum Albumin stays steady at 4.0-4.2

    I hope that is not the case. One windmill I tilt at is the ‘one-size-fits-all’ dialysis model ... all patients are NOT the same. Individual dialysis prescritions are needed to overcome individual needs and it should be possible to accommodate a range of dialysate variations in any unit. In my view, it is indefensible not to do so, if dialysate or other prescription individualizations are indicated – as they very often are. - I believe the vast majority of nephs would agree with you. However, in corporate dialysis, unfortunately, compromises are made. I know the unit provides 2.0/2.5/3.0 Ca concentrations. Just not sure about 3.5. While I go to an Emory University Healthcare dialysis facility, the day to day management has been contracted out to a for-profit company. Still, I believe the nephrologists have more say in this situation than within a full corporate environment.

    Once again, Dr. Agar, thank you for your thoughts. You are providing an invaluable resource for patients.

    Cordially - Frank Moiger (NoahVale)
    Last edited by Noahvale; May 5, 2012 at 03:10 PM.

  10. #10
    Join Date
    08-17-04
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    Default Re: Mysterious hypotension

    Moosemom, did Dr. Agar's advice help Desert Dancer? It's been a couple of months (almost), and we're curious...

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